本手稿回顾了维持反刍动物妊娠黄体（CL）的机制。在哺乳动物中,CL中剩余细胞的排卵和黄体化是由于促黄体生成激素（LH）的激增。在牛身上,LH脉冲的持续分泌对于在发情周期（LH脉冲）期间CL的完整发育和功能至关重要，然而,关于妊娠d20后CL的少数研究并未表明LH对于维持妊娠CL至关重要。维持反刍动物妊娠CL的第一步是克服导致非妊娠反刍动物CL消退的机制（牛的d18-25；绵羊的d13-21）。这些机制具有涉及催产素诱导的前列腺素F2α（PGF2A）脉冲的子宫成分和涉及孕酮产生减少和黄体细胞死亡的黄体成分。胚胎干扰素-tau（IFNT）在抑制妊娠早期PGF2A的子宫分泌（绵羊中的d13-21；牛中的d16-25）和防止黄体溶解方面具有关键作用。IFNT对包括CL在内的其他组织中干扰素刺激基因的表达也有影响，但这些干扰素刺激基因的生理作用尚不清楚。在IFNT期间之后，还有另一种机制维持反刍动物妊娠的CL，因为胚胎IFNT在附着发生时受到抑制，并且滋养细胞的双核/巨细胞开始分泌与妊娠相关的糖蛋白。黄体维持的第二种机制尚未确定，但以局部方式（妊娠同侧）起作用。并保持功能从d25直到分娩前。介导妊娠CL后期维持的最可能机制是子宫血流量增加或子宫-卵巢脉管系统中前列腺素转运体表达减少，防止PGF2A到达CL。最后,探讨了这些想法对牛妊娠流产的影响，强调妊娠CL不适当消退作为牛妊娠丢失机制的重要性。
This manuscript reviews the mechanisms that maintain the corpus luteum (CL) of pregnancy in ruminants. In mammals, ovulation and luteinization of the remaining cells in the CL are due to a surge in Luteinizing Hormone (LH). In cattle, continued secretion of pulses of LH is essential for full development and function of the CL during the estrous cycle (LH pulses), however, the few studies on the CL after d20 of pregnancy do not indicate that LH is essential for maintaining the CL of pregnancy. The first essential step in maintaining the CL of pregnancy in ruminants is overcoming the mechanisms that cause regression of the CL in non-pregnant ruminants (d18-25 in cattle; d13-21 in sheep). These mechanisms have a uterine component involving oxytocin-induced prostaglandin F2α (PGF2A) pulses and a luteal component involving decreased progesterone production and luteal cell death. There is a critical role for embryonic interferon-tau (IFNT) in suppressing the uterine secretion of PGF2A during early pregnancy (d13-21 in sheep; d16-25 in cattle) and preventing luteolysis. There are also effects of IFNT on the expression of interferon-stimulated genes in other tissues including the CL but the physiologic role of these interferon-stimulated genes is not yet clear. After the IFNT period, there is another mechanism that maintains the CL of pregnancy in ruminants since embryonic IFNT is inhibited as attachment occurs and trophoblastic binucleate/giant cells begin secretion of pregnancy-associated glycoproteins. The second mechanism for luteal maintenance has not yet been defined but acts in a local manner (ipsilateral to pregnancy), and remains functional from d25 until just before parturition. The most likely mechanisms mediating later maintenance of the CL of pregnancy are increased uterine blood flow or decreased prostaglandin transporter expression in the utero-ovarian vasculature, preventing PGF2A reaching the CL. Finally, implications of these ideas on pregnancy loss in cattle are explored, highlighting the importance of inappropriate regression of the CL of pregnancy as a mechanism for pregnancy loss in cattle.
